The chimera‐type galectin‐3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus

Abstract

Problem From conception, a delicate regulation of galectins, a family of carbohydrate‐binding proteins, is established to ensure maternal immune tolerance in pregnancy. Though galectin‐3 (gal‐3), the only chimera type galectin, is abundantly expressed at the feto‐maternal interface; the physiological role of this lectin during pregnancy remains to be fully elucidated and requires further investigation. Method of study In this study, we analyzed serum gal‐3 levels during the course of healthy gestation. Trophoblast functions were evaluated upon gal‐3 exogenous stimulation using trophoblastic cell lines (e.g. HIPEC65, SGHPL‐4 and BeWo cells). Finally, we investigated variations in peripheral gal‐3 levels associated with the development of spontaneous abortion and gestational diabetes mellitus (GDM). Results Gal‐3 circulating levels increased as normal pregnancy progressed. In vitro experiments showed that exogenous gal‐3 positively regulated trophoblast functions inducing invasion, tube formation and fusion. Compared with normal pregnant women, circulating gal‐3 levels were significantly decreased in patients who developed GDM. Conclusion Our results reveal a physiological role for gal‐3 during pregnancy, promoting proper trophoblast functions associated with healthy gestation. GDM is associated with a failure to increase circulating gal‐3 levels late in gestation. Thus, dysregulation of gal‐3 may indicate a contribution of the chimera‐type lectin to this adverse pregnancy outcome.